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The relationship between genes and cancer is a complex one, and numerous studies have been conducted to establish the role of genetics in cancer. While there are some types of diseases that are inherited and run in a given family, most cancers are not clearly linked to genes inherited from family ties. Most cancers are caused by gene changes that occur during the course of a person’s life. Through advancement in genetics and molecular biology, human’s knowledge on the working of cells in the body has improved. This has helped people to understand better the role of genetics in cancer and how cells in the human body to cause cancer. Biological advancements have also enabled how inherited genes can help speed up the development of cancer in an individual.
Several studies have been conducted by professionals in different fields of medicine to help expand the knowledge on the role of genetics on cancer. A study by Pomerantz et al. is one such studies that look to identify the role of genetics on some given types of cancer. The authors of the article, “The genetics of cancer risk,” conducted a study review to establish what role genetics plays in causing or speeding up the development of cancer, with a specific focus on prostate cancer. This study was carried out due to the numerous links to some genetic variation as risk factors for ovarian cancer. While the article reviews the role of genetics in the development of prostate cancer, the same principles apply for any cancer as well as any generic trait. The article reviews the discoveries that have been made on the genetic basis of inherited cancer risk. It provides for how these discoveries contribute to the knowledge of cancer biology and also inform the management of patients with cancer.
The study first reviews how family history increases the risk of cancer. According to the article, a meta-analysis that reviewed 33 epidemiologic studies determined that individuals having a first-degree relative who has had prostate cancer are at approximately 2.5-fold lifetime risk of the disease. This risk increases for individuals having more than one relative affected by prostate cancer. For such individuals, the risk is at approximately 5-fold, making their risk two times greater than for individuals with only one relative affected by prostate cancer (Pomerantz et al., 2011). The study further reinforces these trends with analyses form both the Swedish Family-Cancer Database as well as the Health Professionals Follow-up Study (HPFS). Similarly, family history is a significant risk factor for common types of cancer, like colon cancer and breast cancer.
While such trends do show that inherited genetic factors lead to the development of cancer in an individual, the article also identifies their limitations in that they are do not have a clear distinction between the genetic and non-genetic factors that lead to increased risk factor for cancer in a given family. This is due to the fact that the components of the disease do not have to be inherited as family members tend to share the same lifestyles and exposures that could lead to the trends in the disease within the same family (Pomerantz et al., 2011). However, focusing family history on twin studies strongly implicates genetic heredity in susceptibility to cancer. The article identifies that the first genes to be associated with the inherited risk of cancer were discovered by the use of the Mendelian approach. This approach focuses on families in which a particular type of cancer has been transmitted in an identifiable pattern. This method has enabled the discovery of causative genes that are linked to diseases such as BRCA-associated breast cancer (Pomerantz et al. 2011). This method uses a linkage analysis to establish risk loci. Linkage analysis has been applied to prostate cancer, and risk loci have been reported. However, while linkage mapping has produced several proofs of genetic inheritance, the method fails to identify risk loci associated with other common types of cancer.
Other than Mendelian approaches that focus on patterns that segregate according to precise patterns that are seen within families, the article also reviews more complex methods of determining the role of genetics ion cancer. In order to identify genetic modifications associated with complex phenotypes, the focus of the article shifted from hereditary genetics to more common genetic variations in unrelated populations (Pomerantz et al., 2011). The study identifies the use of less biased approaches to understanding the role of genetics in cancer. This involves the use of Genome-wide association studies (GWAS) to scan the genome for polymorphisms that are associated with the trait of interest (Pomerantz et al. 2011). GWAS compare the genes of affected members and unaffected members while comparing the allele frequency among the individuals. The use of GWAS, unlike the use of family history, is unbiased and produces better results in showing the role of genes in cancer.
The study shows that functional consequences of inheriting a risk allele are not readily apparent. More insight into mechanisms underlying associations between risk loci and cancer is needed to increase the understanding of genes and cancer. According to the reviews by the article, inherited gene variations can influence phenotype in different ways. They can directly alter the gene transcription and amino acid sequence or affect the regulation of gene activity, for example, by affecting gene splicing. They can also disrupt the transcription of non-coding RNAs (Pomerantz et al., 2011). The study concludes that GWAS techniques have really helped identify the role of genes increasing the risk of cancer for individuals. However, GWAS data does not reflect the full complement of factors associated with inherited risk. More studies need to be conducted on the role of genetics in both inherited and inherited types of cancer.
Work Cited
Pomerantz, Mark M., and Matthew L. Freedman. “The genetics of cancer risk.” Cancer journal (Sudbury, Mass.) 17.6 (2011): 416.